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p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-ren...

p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-ren...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_b860fba9de8448de8c15f0811ec7cae9

p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-renewal of TICs

About this item

Full title

p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-renewal of TICs

Publisher

London: Nature Publishing Group UK

Journal title

Nature communications, 2020-06, Vol.11 (1), p.3084-16, Article 3084

Language

English

Formats

Publication information

Publisher

London: Nature Publishing Group UK

More information

Scope and Contents

Contents

Tumor-initiating stem-like cells (TICs) are defective in maintaining asymmetric cell division and responsible for tumor recurrence. Cell-fate-determinant molecule NUMB-interacting protein (TBC1D15) is overexpressed and contributes to p53 degradation in TICs. Here we identify TBC1D15-mediated oncogenic mechanisms and tested the tumorigenic roles of...

Alternative Titles

Full title

p53 destabilizing protein skews asymmetric division and enhances NOTCH activation to direct self-renewal of TICs

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_doaj_primary_oai_doaj_org_article_b860fba9de8448de8c15f0811ec7cae9

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_doaj_primary_oai_doaj_org_article_b860fba9de8448de8c15f0811ec7cae9

Other Identifiers

ISSN

2041-1723

E-ISSN

2041-1723

DOI

10.1038/s41467-020-16616-8

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